Abstract: Of the 35 patients with mutations at T2, 80% had M184V/I, 65.7% Y181C, and 48.6% (54.8% excluding those not on Tenofovir) had K65R mutations.
Abstract: The high rate of K65R and TAMs could compromise second line regimens including NRTIs.
Conclusion: The second-line regimens recommended were appropriate, however, the high rate of the K65R and TAMs is likely to compromise second-line drugs containing other NRTI backbone.
Result: Of the 35 patients with mutations at T2, 80% had M184V/I, 65.7% Y181C and 48.6% (54.8%, if those not on Tenofovir are excluded) had K65R mutations.
Result: The 22 cases experiencing virologic failure presented with the following DRMs: M46I, F53LY, I54LTV, G73ST, L76V, V82AT, I84V, I185V, N88D, and L90M for PIs; L100I, K103NS, V179F Y181C, G190AS, V106A, K103N, and P225H for NNRTIs; and
HIV-1 Drug Resistance Mutations: Potential Applications for Point-of-Care Genotypic Resistance Testing.
Result: About one-half of the viruses with K65R did not have M184V, making K65R the second largest contributor to the cumulative proportion of viruses with a major NRTI DRM.
Result: Fig 2 shows that in viruses from individuals in LMICs with intermediate or high-level NRTI resistance following VF on a first-line NRTI/NNRTI-containing regimen, the most common major DRMs were M184V (91.5%) and M184I (3.7%), K65R (9.8%), and the TAMs K70R (14.6%),
[Analysis of HIV-1 drug resistance among 1 922 individuals experiencing virological failure of first-line antiretroviral therapy in Henan province].
PMID: 26833003
2015
Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine]
Abstract: K65R/N and Q151M complex existed in 23 and 4 patients, respectively.
The emergence of drug resistant HIV variants at virological failure of HAART combinations containing efavirenz, tenofovir and lamivudine or emtricitabine within the UK Collaborative HIV Cohort.
Abstract: 21 cases of K65R were detected over the course of follow up, giving an overall event rate of 0.21 (95% CI: 0.12-0.31)/100 person years follow up (PYFU).
Abstract: 47 of these episodes were preceded by resistance tests showing development of K65R or M184V mutation and were hence excluded.
Abstract: CONCLUSIONS: We have not found evidence of an increased risk of development of M184V and K65R in patients exposed to 3TC.
Abstract: METHODS: In this study we analysed linked data from the observational UK Collaborative HIV Cohort (CHIC) Study and UK HIV Drug Resistance Database (HDRD) to investigate the rate of development of K65R or M184V resistance mutations in patients failing on combinations containing tenofovir (TDF) and efavi
HIV-1 virologic failure and acquired drug resistance among first-line antiretroviral experienced adults at a rural HIV clinic in coastal Kenya: a cross-sectional study.
Method: In this study, HIV-2 resistance mutations were identified using the list generated by the 'Collaborative HIV and Anti-HIV Drug Resistance Network', leading to the following mutations in reverse transcriptase - K65R, D67G/N, N69S/T, K70N/R, L74V, V111I, Y115F, M184I/V, Q151M, S215A/C/F/L/Y, K223R; and in protease - V47A, G48V, I50V, I54L/M,
Characteristics of HIV-1 natural drug resistance-associated mutations in former paid blood donors in Henan Province, China.
Discussion: Results from the HIV-1 drug resistance mutation research by the International AIDS Society-USA (updated in March 2013) have revealed that PI resistance mutation sites are L10I, K20M, V32I, M36I, M46I/L, I47V/A, I50V, Q58E, A71V, G73S, V82A/F/T, I84V, L89V,L90M; NRTIs resistance mutations are M41L, A62V,
ViMRT
HIV mutation literature information.
PMID: 
2015
PloS one
